Patients with diabetes and metabolic disorders have excess mortality after myocardial infarction (MI). Their mitochondrial function is often abnormal, and can be measured with phosphorus magnetic resonance spectroscopy (PMRS). Participation in a program of cardiac rehabilitation and secondary prevention (CRSP) reduces post-MI mortality, but typically involves only aerobic exercise and may not sufficiently improve mitochondrial function. An integrated assessment of skeletal muscle would potentially be useful to assess the impact of aerobic plus resistive exercise post-MI.

An integrated protocol of skeletal muscle 31P spectroscopy with fat quantification is feasible in patients starting cardiac rehabilitation, and may help improve understanding of cardiometabolic interactions that are not evident from cardiac measures alone.

Figure 1

A) Phosphocreatine (PCr) concentration is depleted with rapid resistive extremity exercise and returns to baseline levels within a recovery period (τ), which is a well-established biomarker of mitochondrial oxidative function. A representative recovery curve is shown. B) Comparison of PCr recovery times demonstrates sequentially poorer mitochondrial oxidative capacity in control subjects, non-diabetic and diabetic patients. C) A representative quantitative fat image acquired through the leg illustrates the measurement of intramuscular lipid. D) Comparison of results indicates sequentially higher skeletal muscle fat content in control subjects, non-diabetic and diabetic patients.

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